Dear Jessica,

Firstly, I apologise that I had not seen your response to my reply until today and should have actively looked for it but failed to.

I will respond in a big picture way before addressing your questions many of which relate to how a virus could spread.

The reason I believe that virus travels rapidly across the world is based on many observations:

1. Every variant of SARS-CoV-2 has been detected globally within a very short period of time - it was not just the first one.

2. For influenza each winter this is also true - spikes of illness caused by the same genetic variant of virus well before close contact transmission alone could have accounted for spread.

3. Whole genome sequencing of SARS-CoV-2 has also taken place globally - crazy numbers have been sequenced - which confirm that these variants spread rapidly across the globe.

4. Aerosols survive at least 16 hours in the air and spread therefore occurs over long distances and would be particularly successful at night when there is no uv e.g. the spread that was correctly predicted based on air currents between apartment blocks.

5. Viruses - in large quantities - have been deteceted in the air far from humans e.g. above the mountains in spain and viable virus over the sea.

6. Other viruses have spread long distance e.g. foot and mouth from France to the Isle of Wight and pig coronaviruses travelling 10 miles.

7. SARS-CoV-2 reached the Antarctic research base despite no possible direct transmission and infected Argentinian fishermen at sea 7 weeks after their departure.

8. The vaccines caused immune suppression in the first two weeks which led to a markedly higher risk of covid infection. The risk was immediate. Hospitalisations occurred that day. That implies there is continuous exposure to virus and our immune systems (particularly the impenetrable mucus layer of the respiratory tract) protect us.

9. As I said in my last response, “the susceptibility appears to come in waves. I say this for two reasons. Firstly, the hospitalised population had peak infections at exactly the same time as the infections peaked in the community. If person to person spread was the cause of the peak then we would expect the hospital peak to occur after admissions from the community -that never happened. Secondly, the peaks happen at predictable times of year.” A wave of susceptiblity passing through the population makes sense of this but susceptibility to what? Virus in the air is still part of the equatoin.

10. Where does the virus come from? Exponential growth is key to understanding this. A single viral particle will replicate 10 fold in 36 hours. That means that in in a fortnight it will have increased 10 fold 9.33 times (14*24 hours / 36 hours = 9.33). That would take one particle to 2.1 billion particles. It would be lower with an effective immune response but you get the idea. A tiny number of people when infected can produce enough virus to potentially infect vast numbers.

11. The amount of virus needed to cause an infection is lower in SARS-CoV-2 than for other viruses. According to the UK government, “sampling of environments where people have influenza or Monkeypox show far more viral RNA than for SARS-CoV-2, yet the outbreak data indicate that both are much less transmissible. This suggests that a lower viral dose is needed to initiate a SARS-CoV-2 infection than for these other diseases.” For other infections, a single virus particle has been shown to be enough to cause infection in one laboratory study. Other studies show that single digit numbers are enough such that a single virus laden aerosol would more than suffice. An individuals susceptiblity is the key variable as to how much virus causes infection. Higher doses can overwhelm immune defences in those who might otherwise have been immune - hence the almost 100% success rate when very high doses were used for immune challenge experiments for vaccine testing. (More than a third of those infected developed symptoms within a day and the mean time to symptoms was only three days, or twelve doubling periods showing how excessive the dosing was).

Now to answering your specific questions:

Do you operate from the assumption that SARS-CoV-2 was “created” or tinkered with at WIV, irrespective of whether another lab may have been working on a version thereof?

No - I am open minded. I have no assumptions about where the work took place. I do think that the virus spread began in Wuhan though in autumn 2019.

You stated “anyone could have mimicked that work [at WIV] as a decoy.” By ‘anyone,’ do you mean ‘any other virus lab anywhere else'? What do you mean by 'decoy'? I’ve used 'decoy' to describe both SARS-CoV-2 and the COVID shot, so I’m comfortable with the term, but I don’t assume your meaning aligns with mine. 'Decoy' implies intent—do you mean to convey intent? If so, could you elaborate?

I was only stating what is possible - the rest is speculation. I have no evidence of intent or lack of it and remain open minded.

You propose a mechanistic explanation for how the 'manmade' virus spread once it was 'out there.' However, like Matt Ridley, you haven't addressed how the Antagonist may have moved from its point(s) of origin to everywhere else and are instead asking the audience to simply accept that the virus 'got out there somehow.' In either a leaked/escaped or released scenario, what exactly are you envisioning could have occurred? What possibilities exist?¹ For example, is the idea that infected lab workers left the lab, expelled the virus into the air, and from there, 'it' took off? Given the conditions and timing you’ve suggested, it seems you would have to believe that something was either sprayed or released into the air at one or more locations—or delivered through a very direct method. Can you clarify your position?

If you're reluctant to propose possible scenarios, perhaps you could instead share what you believe could not have happened?

I hope my explanation above covers this. All that is required is for someone to be infected. From there, exponential replication of virus being breathed into night air is all that’s needed for spread. That does not preclude a deliberate release.

I don’t see a direct answer to my question about whether you believe Gain of Function is capable of producing agents can at least match nature. Based on your response about the virus causing a specific and unique disease, I assume your answer is yes. (Please let me know if I am mistaken.)

Yes - you are not mistaken.

I currently believe that a newly-named coronavirus was not suddenly, quickly, or exponentially spreading from person to person or circulating in the air [in late 2019/early 2020]. When I say “spread” I am referring to the WHO’s (abrupt and unsubstantiated) claim in January 2020 that human-to-human transmission of the virus was occurring. Am I correct that you currently believe a newly-named manmade coronavirus was spreading in the air in late 2019/early 2020 - beginning on/around October 2019 - and (to a lesser extent) transmitting between humans?

I believe there was human to human transmission but that it was driven by long distant aerosol spread. Close contact tranmission occurred but was not the driver of the trajectory of any wave.

Here’s my layperson’s summary of your mechanistic proposition for spread once the virus was “out there” from the lab(s). Please let me know if this is correct.

The primary driver of SARS-CoV-2 spread, in your view, is aerosol transmission. This must be the case, you assert, because 'spread was too rapid, continued throughout lockdowns, reached remote places, and was unhindered by masking.' Aerosol transmission occurs when people exhale virus-containing particles into the air, where they can remain for 'very long periods of time.' 'Spread' is extremely fast, and the viruses and its variants 'traverse the world' independently of air travel. Most transmission occurs at night—when people are typically indoors or asleep.

Yes. Dosage of virus in the air will also rise and fall with a wave.

You believe SARS-CoV-2 was “spreading in a low-grade way” before March 2020. What does “spreading in a low-grade way” mean? In the air at a low prevalence/concentration and not being inhaled and expired at a high rate by many living things? Or, in the air, widely-”spread”, but not impacting surveillance, death, or any other kind of data for other reasons? Am I correct that your evidence for believing in this “low-grade spread” is the results of antibody testing/seroprevalence studies?

The conventional model of viral attack is based on the premise that we are all susceptible and exposure to an infected person determines outcome. This fails on many counts but the key is that the exponential spread that should result from that is always capped such that only 5-15% of the population are infected in each wave. The evidence points to the exponential rise being related to a seasonal surge in susceptibility. Between these seasonal surges spread is still possible but the wave of susceptibility is not occurring. Spread can continue in a chain but does not take off exponentially. Edgar Hope Simpson carefully detailed how this occurs for influenza. Every source of public health data from the antibody testing you mentioned (figure 1 here) to ambulance calls for people with breathing difficulties to the number of respiratory infection outbreaks of any cause in care homes all supports this. PCR testing, while flawed, also supports this. There was extensive testing done in Jan and Feb 2020 in UK but the percentage positivity only rose in line with symptoms in people who later developed antibodies, peaking 10 days later as would be expected as testing was largely in hospitals detecting people admitted 10 days into their infection.

You contend SARS-CoV-2 was “new”/newly-introduced to humans/their environment at some point in time and - had it gone ‘unfound’, unannounced, and “un-reacted to” - many places would’ve seen an out-of-season flu spike in outpatient and emergency department visits for influenza-like illness in spring 2020. What is your rough estimate for this spike (% over normal for time of year)?

Spring is not out of season for flu in the UK, it is just not peak season. There was clearly a big difference in infection mortality rates that could not be accounted solely for by a) age and comorbidity differences and b) differences in geographical susceptiblity e.g. Germany and Eastern Europe had no spring 2020 wave but did have a spring 2021 wave that the UK did not have. I have not been able to unpick the relative contributions of policy induced deaths and viral deaths from the total excess. Nor viral deaths that were inevitable from those that were a consequence of policy i.e. people deterred from seeking healthcare, large numbers of emergency healthcare workers forced to isolate, over use of ventilaiton and end of life drugs etc. I do think that even after eliminating those factors there was a virus which was causing more harm than an average seasonal respiratory virus. I know plenty of people who were sicker with this than normal seasonal respiratory viruses. Of course that will mean that more frail people would succumb too.

Do you believe the off-season ILI spike would have been accompanied by an increase in respiratory disease deaths? Why or why not? (If yes, what is your rough estimate for the rise? Would the rise have materialized in all-cause mortality for those weeks?)

Yes - I can’t estimate the rise. Yes there would be all cause excess mortality - but the overall excess for covid including all the policy induced deaths is the same per 100,000 people as has been seen in many previous influenza seasons. It has to be lower than that.

I didn’t initially ask about testing because the footnote quoted above says “and not tested for anything,” meaning SARS-CoV-2. Obviously, flu testing was happening; in the U.S. (and UK too, I think), the “surveillance season” is October through May. You are assuming more ILI in the form of visit data AND flu tests being given, but NOT in flu tests coming back positive, correct?

Influenza like illness did increase based on symptom surveys. The rate doubled from week 9 to week 12. I have not seen data on the number of flu tests being done. Flu tests were not coming back positive.

Which places (cities/regions) do you think would have seen such a spike - and why?

I presume you mean spike in influenza like illness. I would have thought the spike would align with what was observed by way of covid i.e. Eastern Europe including Germany, South East Asia and Australasia, the middle states of USA would not have seen a spike.

You believe COVID-19 is a “characteristic disease” caused by SARS-CoV-2.² Reviewing the long list of associated symptoms, is it your assumption that this “characteristic disease” would have been observed or characterized as such without a virus name, test, etc.? (Would it have been detected clinically?)³

Yes, it was observed and characterised clinically. Here is a frontline critically thinking GP describing his observations before anyone told him what to think.

Feel free to follow up with more questions if you think I am missing something.

All the best,
Clare